If You Want To Regrow Hair; Read This Article!!!!!!!!!!!!!!!

[elan164]

And why would there be a conspiracy to repress the true cause of male pattern baldness, when whoever finds a 100% cure for hairloss will have fame and fortune beyond their wildest dreams?!!

:baaa:

Well obviously you didnt think about this statement before you wrote it. A patient cured is worth less than a patient that has to take medication for the rest of their life. If a cure came out think of ALL the products out there that would no longer be tried/used. This is serious money.

The body is a complex unit. One has to think that all the chemicals in the air, water, food etc has some role in this, atleast i do.

 

[Quantum Cat]

Well obviously you didnt think about this statement before you wrote it. A patient cured is worth less than a patient that has to take medication for the rest of their life. If a cure came out think of ALL the products out there that would no longer be tried/used. This is serious money.

that's still conspiracy talk. The hairloss industry isn't controlled by just one person or company. If a company found a guaranteed cure for male pattern baldness do you really think that they'd suppress it because they're worried that their rival companies might lose a lot of money? If Merck found the holy grail 'cure' (which probably doesn't exist anyway) would they be worried that their propecia sales would take a dip if they put the 'cure' on the market? I doubt it

The body is a complex unit. One has to think that all the chemicals in the air, water, food etc has some role in this, atleast i do.

All those things certainly have a role in general body and mind health, and hair health, but their impact on male pattern baldness is probably miniscule at best. That's why you see super-fit athlete health freaks who are balding or totally bald.

 

[mykal_P]

yeah and a cure would not mean an end to sales elan, as you would need to still buy something to combat yer natural genetics on a regular basis or go back into losing.

As I've stated before, if the "estrogen being bad" is true, then why aren't guys trying to become females via "female hormone" therapy losing hair in great amounts?

 

[wesleyBelgium]

break down the receptors on the hairfollikels and you have your hairsolution , not for regrowth but to stop hairloss...

i also dont believe that less estrogens and more androgens are the solution sinds this hormones bind to every receptor in your body , hairloss, prostate problems , tumors , it all works with receptors....

cant a high concentrated dose of curcumin on a liposomes vehicle be a solution ?
or asc-j9 if you can get the stuff orderd...

transsexuals dont lose any hair... most of the time on meds to block androgens they regrow hair... so less androgens, and more estrogens , and still more regrowth , if you look on it , estrogens arent bad for hairloss...

 

[S Foote.]

MisterE and S. Foot, I don't even bother to read your posts since I know they are full of sh*t and misinformation.
Keep thinking whatever you want but keep in mind that you do not fool anyone except, maybe, a few retarded people.
The conspiracy theory is f****ing stupid, too. A company would make some motherfucking money with a cure for male pattern baldness.

Just to clear up a possible misunderstanding here for the people reading this thread.

I jumped into this thread purely to question Bryans statment on a particular issue.

For the record i don't agree with MisterE's idea's about the mechanism of male pattern baldness. I have raised questions with him in PM's in this regard.

So please, if anyone has a point to make about my views thats OK i will defend them, but don't blame me for other peoples opinions!

S Foote.

 

[moxsom]

But why do you think that androgens are the main cause of hair loss in men when androgens actually decrease as men age?

That question comes up occasionally on hairloss sites like this one (or related questions, like "Why do some people start balding relatively late in life, even though their androgen levels are highest in their late teenage years, or early 20's?"). I'm going to answer that question for all the other readers who may be wondering the same thing (you've demonstrated to me that you don't listen to what people tell you). There are at least TWO important reasons for why it can take a long time for a man to develop balding, even though his overall androgen levels may be slowly declining:

1) Damage to hair follicles from androgens is cumulative, and can sometimes take YEARS to develop. It doesn't just happen overnight.

2) Scalp hair follicles can become more and more sensitive to androgens over a period of time (years). They don't simply change from being relatively insensitive to androgens (like they are, prior to puberty) to being fully sensitive to androgen the day that puberty hits. It's a gradual process of becoming more and more sensitive to androgens. The very slowly declining average levels of androgens in aging men by itself isn't sufficient to stop the balding process.

This speculation of yours has a very big flaw Bryan, as i have pointed out to you before. There have been at least two times in past posts where i have explained this flaw to you, but you have refused to answer my point.


So here it is again.

What you try to claim here is impossible, given what we now know about the hair cycle and stem cells.

I would advise you to read this article by Elaine Fuchs and her team.


http://newswire.rockefeller.edu/index.p ... ine&id=881

In a nutshell, quote:


"For a new round of hair growth to begin, stem cells in the hair follicle must receive a signal to divide. In response to this signal, the hair follicle regenerates first by growing downward through the skin’s middle layer, the dermis, and then producing the specialized cells that form the hair. After a period during which the hair grows longer, stem cells stop dividing, and the hair follicle gradually retracts again. There is then a period of rest and the cycle repeats."

So stem cells create "NEW" hair producing cells every hair cycle.

You claim that these cells take "YEARS" to become androgen sensitive, longer in fact than the average human scalp hair cycle.

male pattern baldness follicles still cycle, so why dont we get normal hair again from these "new" follicles, at least for the years it takes them to become "sensitive" to androgens? (according to you).

A proper scientific response please Bryan.

S Foote.

Okay I'll bite. Have you ever read published work by Dr. Fuchs? it's nice that you have a news article about her research, but looking at actual research gives you a much clearer picture of whats going on.

The fact that stem cells create "NEW" hair producing cells every cycle is correct, but your theory is way off. Every person is born with between 80k and 150k terminal hairs on your scalp, and each of these hairs go through cyclic asynchronous transformations.

Now here is what you must understand, the Dermal Papilla cells of each hair bulb does not ever get created nor destroyed in these cyclical changes. During catagen, the DP moves closer to the bulge, pigmentation is stopped and eventually the hair shaft is released. When anagen starts again stem cells differentiate into at least 8 different cell lines, forming the ORS, companion layer, Henle’s layer, Huxley’s layer, cuticle of the IRS, cuticle of the hair shaft, shaft cortex, and shaft medulla. Unfortunately for us, the DP still functions as the main part and determines depth, hair length, thickness, etc.

So yes, stem cells of the hair bulge create most hair cells but do not actually recreate the dermal papilla which controls cycling, length or thickness.

Androgen mediated damage affects the Dermal papilla, therefore affecting the things I have mentioned above. Although Bryan and I disagree that androgens can also effect different cells in the scalp, its all because of androgen mediated damage S. Foote and MisterE.

A great article to read on stem cell cycling is:
Biology of the Hair Follicle: The Basics
Seminars in Cutaneous Medicine and Surgery, Volume 25, Issue 1, March 2006, Pages 2-10
Karoline Krause, Kerstin Foitzik

If you do not have access, drop me your email and I will send it to you.

 

[S Foote.]

Okay I'll bite. Have you ever read published work by Dr. Fuchs? it's nice that you have a news article about her research, but looking at actual research gives you a much clearer picture of whats going on.

The fact that stem cells create "NEW" hair producing cells every cycle is correct, but your theory is way off. Every person is born with between 80k and 150k terminal hairs on your scalp, and each of these hairs go through cyclic asynchronous transformations.

Now here is what you must understand, the Dermal Papilla cells of each hair bulb does not ever get created nor destroyed in these cyclical changes. During catagen, the DP moves closer to the bulge, pigmentation is stopped and eventually the hair shaft is released. When anagen starts again stem cells differentiate into at least 8 different cell lines, forming the ORS, companion layer, Henle’s layer, Huxley’s layer, cuticle of the IRS, cuticle of the hair shaft, shaft cortex, and shaft medulla. Unfortunately for us, the DP still functions as the main part and determines depth, hair length, thickness, etc.

So yes, stem cells of the hair bulge create most hair cells but do not actually recreate the dermal papilla which controls cycling, length or thickness.

Androgen mediated damage affects the Dermal papilla, therefore affecting the things I have mentioned above. Although Bryan and I disagree that androgens can also effect different cells in the scalp, its all because of androgen mediated damage S. Foote and MisterE.

A great article to read on stem cell cycling is:
Biology of the Hair Follicle: The Basics
Seminars in Cutaneous Medicine and Surgery, Volume 25, Issue 1, March 2006, Pages 2-10
Karoline Krause, Kerstin Foitzik

If you do not have access, drop me your email and I will send it to you.

Yes i have read other papers by Fuchs, so please dont try to patronise me with that kind of remark. My own interest lies in her research on the involvement of the Wnt's pathway in hair follicle expansion. I believe that this supports the involvement of normal contact inhibition in the in-vivo size of hair follicles.

It is late here in England, so i will be brief now.

OK, lets say that the DP cells "DO" have a continuous line, and so they may be able be effected by androgen exposure over a long period of time.

Would you like to explain how such a long period of time could result in cells changing from non responsive, to being fully responsive just by long term exposure to the very substance (androgens), that they "dont" respond to in the first place? Wheres the precident in recognised hormone physiology? Tell me how this works?

Secondly, if you are claiming such a long period of androgen exposure is neccessary before follicles respond, why do follicles that increase growth in response to androgens (beard, body hair), do so in a more dose related manner after puberty? No extended time period here!

Is this yet another "different" action of androgens?

If you are serious about trying to explain the effect of androgens on hair follicles, you have to explain both sides of the coin?



S Foote.

 

[moxsom]

Would you like to explain how such a long period of time could result in cells changing from non responsive, to being fully responsive just by long term exposure to the very substance (androgens), that they "dont" respond to in the first place? Wheres the precident in recognised hormone physiology? Tell me how this works?

Sure, I would love to explain it to you. It's not the long term exposure to the androgens that makes the dermal papilla from non-responsive to responsive. It's the androgen receptors (although androgens can stimulate androgen receptor production). People with more sensitive androgen receptors will be victims of male pattern baldness. also note that the amount of androgen receptors can increase over time.

The androgens start binding to androgen receptors soon after puberty (DHT has a much higher affinity for binding then any other androgen). Once receptors receive this signal they can release transcription factors into your cell and actually alter genetic expression of you dermal papilla. For example the dermal papilla will now produce more TGF-B, which cause damage to surronding cells. Now it doesnt happen in one bout, the dermal papilla may undergo only a little cellular damage which you do not notice. Now this damage can will accumulate over time, rendering your hair follicle producing more and more anti-growth factors. Remember a regular hair usually goes from anagen to catagen in 2 - 6 years.

Secondly, if you are claiming such a long period of androgen exposure is neccessary before follicles respond, why do follicles that increase growth in response to androgens (beard, body hair), do so in a more dose related manner after puberty? No extended time period here!

Is this yet another "different" action of androgens?

If you are serious about trying to explain the effect of androgens on hair follicles, you have to explain both sides of the coin?

It's not that much different how androgens bind to the different hairs. Except that these hairs (beard, body) are not presently terminal but only become terminal after androgens bind to the receptors. These hairs do not seem to be damaged by androgens after they become terminal. For what reason, I am unsure, but they do differ from hair follicles in that they were not orginally terminal soon after birth.

It seems to happen alot quicker perhaps because they are VERY sensitive to androgens, and probably were necessary in our evolutionary history to tell people we were a) ready to mate (pubic hair) and b) a strong male who could fend off intruders etc (facial hair).

Also you can note that the facial hair you had at 14 was not the facial hair you had at 25. So there is a bit of exended time period, albeit not usually as long as androgenic alopecia. The same as body hair, you will notice men in their 60's have much more body hair then a 15 year old male.

 

[Bryan]

I dont think thats going to fool anyone here Bryan.

The particular point in question is clearly answered by the scientific evidence available.

You claim that it takes years for follicle cells to become sensitive to androgens, the follicle stem cell studies prove that your claim is not possible.

Really? How do they do that?

I think the poster "moxom" gave a good reply to you, demonstrating to you that BY NO MEANS do those stem cell studies explain step-by-step everything that happens to hair follicles. There are still large gaps in our knowledge of how follicles live and die; your attempt to point to those studies as support for your own eccentric theory is the ploy of a desperate man.

This is a good example of what happens when assumptions are made about scientific evidence, because of a persons own beliefs.

LOL!! Yeah, I've seen some really excellent examples of people who do that!

The in-vitro tests clearly show that follicles known to be destined to become male pattern baldness follicles, are not directly changed into male pattern baldness follicles when "feed" androgens. So people who support the direct theory have to explain this.

No, it certainly doesn't happen in a day or two (did you mean "fed" androgens?). It can take years (you already know that, because I've told you about it over and over and over and over). You keep harping on that irrelevant point, because your own theory has so little going for it.

The only way the direct theory can survive in the light of this evidence, and the evidence that every one can see for themselves (male pattern baldness can take years to develope after puberty), is the assumption that it takes years for follicles to become directly sensitive to androgens.

Yeah, that's what I've been telling YOU, for years and years!

But as we can now see from the stem cell research, this attempt at justifing the failure of the in-vitro tests to support the direct action theory, is also finally refuted.

Wow, you're really desperately grasping at straws here, Stephen. I don't see any "failure" of in vitro tests, at all.

Some will argue that the in-vitro tests "do" show that androgens "directly" support the pre-existing growth characteristics of follicle samples, but so could a lot of other substances!

I'm not sure what you mean.

This is a much different thing from finding out how androgens cause growth changes in the first place?

What the in-vitro studies "DO" prove is that androgens "DONT" create this change directly. Now the stem cell studies also support an "indirect" action of androgens.

:sleep:

Really? How do they do that? (yawn)

 

[S Foote.]

I dont think thats going to fool anyone here Bryan.

The particular point in question is clearly answered by the scientific evidence available.

You claim that it takes years for follicle cells to become sensitive to androgens, the follicle stem cell studies prove that your claim is not possible.

Really? How do they do that?

I think the poster "moxom" gave a good reply to you, demonstrating to you that BY NO MEANS do those stem cell studies explain step-by-step everything that happens to hair follicles. There are still large gaps in our knowledge of how follicles live and die; your attempt to point to those studies as support for your own eccentric theory is the ploy of a desperate man.

[quote="S Foote.":2dxcdhc1]This is a good example of what happens when assumptions are made about scientific evidence, because of a persons own beliefs.

LOL!! Yeah, I've seen some really excellent examples of people who do that!

The in-vitro tests clearly show that follicles known to be destined to become male pattern baldness follicles, are not directly changed into male pattern baldness follicles when "feed" androgens. So people who support the direct theory have to explain this.

No, it certainly doesn't happen in a day or two (did you mean "fed" androgens?). It can take years (you already know that, because I've told you about it over and over and over and over). You keep harping on that irrelevant point, because your own theory has so little going for it.

The only way the direct theory can survive in the light of this evidence, and the evidence that every one can see for themselves (male pattern baldness can take years to develope after puberty), is the assumption that it takes years for follicles to become directly sensitive to androgens.

Yeah, that's what I've been telling YOU, for years and years!

But as we can now see from the stem cell research, this attempt at justifing the failure of the in-vitro tests to support the direct action theory, is also finally refuted.

Wow, you're really desperately grasping at straws here, Stephen. I don't see any "failure" of in vitro tests, at all.

Some will argue that the in-vitro tests "do" show that androgens "directly" support the pre-existing growth characteristics of follicle samples, but so could a lot of other substances!

I'm not sure what you mean.

This is a much different thing from finding out how androgens cause growth changes in the first place?

What the in-vitro studies "DO" prove is that androgens "DONT" create this change directly. Now the stem cell studies also support an "indirect" action of androgens.

:sleep:

Really? How do they do that? (yawn)[/quote:2dxcdhc1]

Same old vague non commital speech from you then Bryan.

You would do well to read Moxsom's response to me, and then try to explain yourself in the same detailed manner. Just repeating over and over again that you have answered my points, doesn't mean you have!

S Foote.

 

[S Foote.]

Would you like to explain how such a long period of time could result in cells changing from non responsive, to being fully responsive just by long term exposure to the very substance (androgens), that they "dont" respond to in the first place? Wheres the precident in recognised hormone physiology? Tell me how this works?

Sure, I would love to explain it to you. It's not the long term exposure to the androgens that makes the dermal papilla from non-responsive to responsive. It's the androgen receptors (although androgens can stimulate androgen receptor production). People with more sensitive androgen receptors will be victims of male pattern baldness. also note that the amount of androgen receptors can increase over time.

The androgens start binding to androgen receptors soon after puberty (DHT has a much higher affinity for binding then any other androgen). Once receptors receive this signal they can release transcription factors into your cell and actually alter genetic expression of you dermal papilla. For example the dermal papilla will now produce more TGF-B, which cause damage to surronding cells. Now it doesnt happen in one bout, the dermal papilla may undergo only a little cellular damage which you do not notice. Now this damage can will accumulate over time, rendering your hair follicle producing more and more anti-growth factors. Remember a regular hair usually goes from anagen to catagen in 2 - 6 years.



[quote="S Foote.":11xqu7zi]
Secondly, if you are claiming such a long period of androgen exposure is neccessary before follicles respond, why do follicles that increase growth in response to androgens (beard, body hair), do so in a more dose related manner after puberty? No extended time period here!

Is this yet another "different" action of androgens?

If you are serious about trying to explain the effect of androgens on hair follicles, you have to explain both sides of the coin?

It's not that much different how androgens bind to the different hairs. Except that these hairs (beard, body) are not presently terminal but only become terminal after androgens bind to the receptors. These hairs do not seem to be damaged by androgens after they become terminal. For what reason, I am unsure, but they do differ from hair follicles in that they were not orginally terminal soon after birth.

It seems to happen alot quicker perhaps because they are VERY sensitive to androgens, and probably were necessary in our evolutionary history to tell people we were a) ready to mate (pubic hair) and b) a strong male who could fend off intruders etc (facial hair).

Also you can note that the facial hair you had at 14 was not the facial hair you had at 25. So there is a bit of exended time period, albeit not usually as long as androgenic alopecia. The same as body hair, you will notice men in their 60's have much more body hair then a 15 year old male.[/quote:11xqu7zi]

Thanks for your detailed respose, but this raises a point that needs to be addressed in more detail.

What exactly is the difference between normal androgen receptors and the alledged "more sensitive" androgen receptors?

Using the normal "lock and key" analogy, the androgen (DHT) combines to the receptor to form the "key". This key then engages with the "lock" in the cell which then creates changes in the cell.

The androgen molecule is the same, so if the receptor is different the "key" would be different. This then implies that the "lock" in the cell has also to be different.

So what is it exactly, and has there been any real world studies to confirm differences in androgen receptors, or indeed different receptor sites?

S Foote.

 

[Bryan]

Same old vague non commital speech from you then Bryan.

You would do well to read Moxsom's response to me, and then try to explain yourself in the same detailed manner. Just repeating over and over again that you have answered my points, doesn't mean you have!

I _did_ answer you in a detailed manner, you flaming hypocrite! I'm sure everybody who has read your posts has noticed that all you EVER do is quote somebody else's posts in full, then add a few separate lines of your own afterwards; to the best of my knowledge and recollection, you have NEVER replied to another person's post on a point-by-point basis, like I do.

Now get off your butt, and answer my post properly!

 

[Bryan]

Thanks for your detailed respose, but this raises a point that needs to be addressed in more detail.

What exactly is the difference between normal androgen receptors and the alledged "more sensitive" androgen receptors?

Using the normal "lock and key" analogy, the androgen (DHT) combines to the receptor to form the "key". This key then engages with the "lock" in the cell which then creates changes in the cell.

The androgen molecule is the same, so if the receptor is different the "key" would be different. This then implies that the "lock" in the cell has also to be different.

So what is it exactly, and has there been any real world studies to confirm differences in androgen receptors, or indeed different receptor sites?

Moxsom can certainly answer for himself, but I'd suggest to you that you start doing some reading and studying of androgen receptors. You can find some very detailed articles about them online which go into some of the known ways that their activity and sensitivity is affected by various chemical and biological factors. That should keep you busy and off the streets for a long time. This stuff is _quite_ complex.

 

[moxsom]

Thanks for your detailed respose, but this raises a point that needs to be addressed in more detail.

What exactly is the difference between normal androgen receptors and the alledged "more sensitive" androgen receptors?

Using the normal "lock and key" analogy, the androgen (DHT) combines to the receptor to form the "key". This key then engages with the "lock" in the cell which then creates changes in the cell.

The androgen molecule is the same, so if the receptor is different the "key" would be different. This then implies that the "lock" in the cell has also to be different.

So what is it exactly, and has there been any real world studies to confirm differences in androgen receptors, or indeed different receptor sites?

S Foote.

Okay, this one will be a bit more difficult to explain. All androgen receptors are BASICALLY the same in structure, but there are MANY pathways happening inside a cell that can influence something like how a receptor acts. Receptor co-activators are a good example of this.

Inui et al. (2007) demonstrated one such co-activator, Hic-5/ARA55, showed extremly high expression in dermal papilla of beard, pubic and bald frontal scalp, where as it was expressed in low amounts in occipital scalp. This is one of the co-factors that has been discovered among others, and i'm sure there are more left yet to be discovered.

There is also a vast amount of papers showing that the shear number of androgen receptors in balding dermal papilla, pubic dp, and beard dp is much higher then non responsive dermal papilla. See Hibberts et al. (1998)

Ellis et al. (2001) showed different polymorphisms in the androgen receptor gene for balding individuals. Our androgen receptors in our scalp may be slightly different from those of non-balding individuals.

So yes, there is a difference in this androgen-sensitive receptor sites.

For more detailed readings see:

Inui, S., Y. Fukuzato, T. Nakajima, S. Kurata, and S. Itami. (2007). Androgen Receptor Co-Activator Hic-5/ARA55 as a Molecular Regulator of Androgen Sensitivity in Dermal Papilla cells of Human Hair Follicles. Journal of Investigative Dermatology. 127:2302-2306.

Hibberts, N.A., A.E. Howell, and V.A. Randall. (1998). Balding hair follicle dermal papilla cells contain higher levels of androgen receptors than those from non-balding scalp. Journal of Endocrinology. 156: 59-65.

Ellis, J.A., M. Stebbing and S.B. Harrap. (2001). Polymorphism of the androgen receptor gene is associated with male pattern baldness. Journal of Investigative Dermatology. 116(3):452-5.

 

[Bryan]

Here's a very brief commentary on androgen receptors from an excellent review article which I've quoted many times in the past: "Male Pattern Hair Loss: Current Understanding", David H. Whiting, MD. International Journal of Dermatology 1998, 37, 561-566. This should give you a brief hint of the chemical complexities that affect the activity of androgen receptors.

Androgen receptors. In men with male pattern hair loss, testosterone and dihydrotestosterone both bind to the androgen receptor in the hair follicle, although dihydrotestosterone binds more avidly. The resulting complex migrates to the cell nucleus and binds to chromatin acceptor sites, affecting the action of ribonucleic acid (RNA) polymerase and subsequent protein synthesis. Differences in the number, type, and affinity of androgen receptors found in different hair follicles may be due to endogenous regional proteins found in hair follicle cells. A peptide inhibitor protein is found in anagen hair follicle cells, and regulates binding to the androgen receptor in a non-competitive way. A converting factor is also found in the anagen follicle cells. It has sulfhydryl oxidative-reductive capacity, and influences binding on the receptor to produce a less active complex.

 

[abcdv12]

I appreciate / thank both Moxsom's and footes comments / knowledge on this topic.

 

[S Foote.]

Thanks for the suggested reading, a lot of which i am aware of.

Perhaps i should be a bit more clear about this.

I can accept that there are "many" differences in "different" follicles in various growth configurations, including their androgen receptors.

But the "direct action of androgens" theory, requires that follicles in the "same" growth position, must be different in some way for male pattern baldness to happen. For example young boys before puberty who are pre-disposed to male pattern baldness, should have a difference in follicles in their "future" male pattern baldness area. At this point the follicles of the scalp are producing the same amount of hair, and show no physical difference.

This is the time when for the direct theory to be correct, it has to show the follicle differences you think are important?

After the transformation does not show causality!

Have there been any studies to show such a difference prior to male pattern baldness?

By the way, i have posted something i think is useful for people who want to know the background to my ideas.

viewtopic.php?f=32&t=56084

S Foote.

 

[Bryan]

This is the time when for the direct theory to be correct, it has to show the follicle differences you think are important?

Have there been any studies to show such a difference prior to male pattern baldness?

Not to my knowledge, although we can already certainly "play the odds" pretty well by testing for androgen receptor polymorphisms. I have no doubt whatsoever that there are other such differences, too, although we may not have the technology or knowledge (yet) to demonstrate them. Eventually, we will.

 

[moxsom]

But the "direct action of androgens" theory, requires that follicles in the "same" growth position, must be different in some way for male pattern baldness to happen. For example young boys before puberty who are pre-disposed to male pattern baldness, should have a difference in follicles in their "future" male pattern baldness area. At this point the follicles of the scalp are producing the same amount of hair, and show no physical difference.

This is the time when for the direct theory to be correct, it has to show the follicle differences you think are important?

Have there been any studies to show such a difference prior to male pattern baldness?

There are studies showing prepubescent children who have been accidently introduced testosterone (usually via a cream that belongs to the father), have had pubic hair growth, and hair growth in other areas that would be stimulated by androgens.

I'm sure if you had enough children (thousands) and introduced them to enough androgens, those who have predisposed androgen sensitivity may show classic male pattern baldness pattern. Of course this is extremly unethical and would never be tested.

But as Bryan said, testing for androgen receptor polymorphisms would be a good idea to catch it early, but there isn't much need of this. It isn't a life threatening disease and those who start available treatments early enough can usually maintain their hair.

 

[mykal_P]

Damn, you guys know a lot about hair. After reading that 3 times to get it, I feel like steven hawking now.

Do you guys think that gene therapy might be effective to alter those bad DP in thinning areas.